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Acute changes in lung mechanics experienced by patients with severe bron-chospasm due to asthma attacks are similar to those observed in COPD during acute exacerbations. However, the pathophysiology of asthma may differ substantially from that of COPD. Increased airway collapsibility due to destruction of the lung parenchyma and loss of lung elastic recoil is a main feature of COPD patients. In asthma, the increases inbronchomotortone, and inflammatory infiltration may

Patient Mechanical Ventilation
Fig. 4. Same patient as in figure 3, ventilated with the same pressure support ventilation (PSV) level but adding 10 cmH2O external PEEP. The inspiratory drive and respiratory muscle effort markedly decreased.

stiffen the airway walls and decrease collapsibility, despite considerable reduction in airway caliber [1, 37]. Additionally, in asthmatic patients, a decrease in lung compliance due to hyperinflation and widespread airway closure has been described, and in these circumstances end-inspiratory plateau pressure may be a better marker of hyperinflation than PEEPi [38]. Moreover, contrary to what occurs in COPD, these factors are usually generalized and reversible with pharmacologic treatment in the case of severe asthma [37].

Current data [37, 39-42] indicate that the ventilatory strategy in acute asthma should favor relatively small Vt and higher inspiratory airflow to preserve expiratory time, in order to minimize hyperinflation, barotrauma and hypotension. This objective could be achieved with inspiratory flows of 80 to 100 l/min (and high peak airway pressure), Vt below 10 ml/kg and alveolar plateau pressures not higher than 25-30 cmH2O [37]. The respiratory rate should be adjusted at relatively low frequencies (about 10 cycles/min), so as to minimize hyperinflation as much as possible and maintain arterial pH in an acceptable range (pH > 7.20).

An important aspect related to mechanical ventilation in asthma is to avoid complications rather than to achieve normocapnia. The low respiratory rates together with small Vt can lead to hypoventilation and severe hypercapnia. Darioli and Perret [40], used controlled hypoventilation in status asthmaticus in a series of 40 patients, and PaCO2 values as high as 90 mmHg were tolerated for more than 24 hours. Complications were a transient hypotension in 40% of patients and barotrauma was observed in only three patients. In a large study by Williams and coworkers [43], it was observed that the risk of hypotension and barotrauma were best predicted by the end-inspiratory lung volume. Indeed, 65% of patients with end-inspiratory lung volume 1.4 l above FRC, had severe complications. Ventilatory adjustments should be ideally based on the level of dynamic hyperinflation, not on PaCO2, so as to maintain the level of dynamic hyperinflation below a safe limit. This corresponds to an end-inspiratory lung volume (above FRC) below 20 ml/kg [44].

Current data in the literature suggest that the risks of increased end-inspiratory airway pressure (reflecting the amount of trapped gas volume above FRC), are much larger than those of permissive hypercapnia. Despite the fact that permissive hypercapnia is contraindicated in the presence of raised intracranial pressure and may cause adverse effects in patients with some forms of cardiovascular disease and patients with preexisting epilepsy, it is probably the safest approach to ventilate patients exhibiting acute severe asthma [39,42, 45].

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